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. 2019 May 5;12(5):e228084. doi: 10.1136/bcr-2018-228084

Unsafe workout: a weak and painful shoulder in a professional volleyball player

Andrea Ermolao 1, Michela Brogi 1, Veronica Baioccato 1, Sara Rovai 1
PMCID: PMC6506065  PMID: 31061176

Abstract

A 29-year-old professional volleyball player started complaining of a dull ache in the right lateral base of the neck. This pain arose during a preseasonal athletic training intense session. After 3 days, he presented deficiency of right scapula adduction, limitation of scapula elevation, right shoulder weakness and local mild pain. He had asymmetrical neckline with drooping of the affected shoulder, lateral displacement and minimal winging of the right scapula. After 1 week, hypothrophy of superior trapezius appeared. An electromyography of right upper limb showed a denervation in the upper, middle and lower components of the right trapezius muscle, due to axonotmesis of spinal accessory nerve (SAN). A subsequent MRI was consistent with muscular suffering caused by early denervation. This case shows idiopathic SAN palsy, likely secondary to an inappropriate use of a weight-lifting machine, where the athlete recovered after an adequate rest and rehabilitation period.

Keywords: pain (neurology), peripheral nerve disease, sports and exercise medicine

Background

Injuries to the spinal accessory nerve (SAN) are often an iatrogenic damage during neck surgery (75%),1 2 while in sports are very rare and less frequent than expected, considering its superficial course in the neck.3 However, early recognition of this injury is critical for the prompt treatment, rehabilitation and return to sport. Further, while in elite sportsmen is infrequent to have an injury after an incorrect training, this condition could be more common in amateur competitors.

Case presentation

A 29-year-old professional volleyball player, without history of recent trauma, surgical procedures or infections, complained of a dull ache in the right lateral base of the neck, exacerbated by digital pressure on the region. The athlete referred that pain was associated with episodes of vagal reaction (asthenia, dizziness, nausea) after training sessions of weight lifting and cold air exposure. After 3 days, he exhibited deficiency of right scapula adduction, mild limitation of scapula elevation, right shoulder weakness, mild pain in the right lateral base of the neck, radiated to the right shoulder, not worsened at night, without sensitivity deficits.

Physical exam revealed a loss of muscle force, with inability to raise the right arm above the level of the shoulder, an asymmetrical neckline with dropping of the affected shoulder, lateral displacement and minimal winging of the right scapula, which was accentuated by arm abduction and external shoulder rotation against resistance. The winging disappeared during forward flexion of the arm. After 1 week, we observed a mild/moderate hypothrophy, that was more evident after 2 weeks. During the following period, the athlete discontinued the training for the upper body, but a moderate pain on the right neck base persisted for about 20 days. Both deep reflexes and strength of upper right limb were normal and no contractures were present. He complained of weakness in the abduction of right arm and inability of scapula adduction, but he could shrug the shoulders, elevate forward the right arm and move the neck in any direction without pain.

Investigations

We performed an MRI of cervical spine and shoulder (3 days after symptoms onset) that showed no signs of mass lesions nor disk disease, a C6–C7 small right paramedian disk protrusion; signs of infraspinatus chronic tendinopathy and acromioclavicular arthrosis, oedema of the spongious bone of the humeral greater tuberosity, at the level of the supraspinatus insertion.

We carried out specific blood tests that excluded infectious diseases (varicella zoster and herpes virus) and degenerative muscular diseases (such as muscular dystrophy, myasthenia gravis). A neck CT scan was performed to rule out vascular problems or masses (thoracic outlet syndrome), but nor vascular ectasia, nor anomalous intramuscular areas of signal enhancement, or significant lymphoadenomegalies were evident. An electromyography of right upper limb showed denervation in the upper, middle and lower components of the right trapezius muscle, due to axonotmesis of SAN. After 20 days, we performed a further MRI that confirmed the mild hyperintense signal short t1 inversion recovery (STIR) in long repetition time (TR) sequences of right trapezius muscle, with light and homogeneous enhancement after contrast (see figures 1 and 2). This clinical picture was consistent with muscular suffering caused by denervation in an early phase. There were not areas of abnormal enhancement in soft tissues or in the spinal roots. Our final diagnosis was idiopathic SAN palsy, likely secondary to mechanical compression.

Figure 1.

Figure 1

MRI image: appearance of denervation of the right trapezius muscle in coronal STIR sequence.

Figure 2.

Figure 2

MRI image: appearance of denervation of the right trapezius in coronal fat saturation T1-weighted sequence, after MRI contrast agent.

Differential diagnosis

  • Paralysis of the rhomboid and serratus anterior muscles.

  • SAN injury.

  • Suprascapular nerve injury.

  • Herniated nucleus pulposus of cervical disks.

  • Progressive neuromuscular disease.

  • Scapular osteochondroma.

  • Herpes zoster or other infections.

  • Thoracic outlet syndrome.

  • Parsonage Turner syndrome.

Treatment

The patient was recommended to abstain from playing volleyball for 3 months and to avoid carrying heavy objects on the affected side. During this time, he was treated with formal physical therapy. The goals of the rehabilitation protocol were to decrease pain, gain/maintain normal Range of Motion (ROM) and a progressive muscle strengthening (trapezius, rhomboids and elevator scapula muscles). Afterwards, he performed a gradual transition to sport-specific movements.

Outcome and follow-up

The athlete completely recovered and returned to play after 3 months, without any complication or relapse.

Discussion

The SAN is the only motor innervation of the trapezius muscle (the major stabiliser of the scapula and an important muscle for shoulder function) and the cranial nerve most susceptible to injury.4 5 The trapezius allows shrugging of the shoulders, retraction of the scapulae, scapular medial stabilisation and scapular rotation.6 7

The SAN is generally injured during sports by traction or cross-body abduction or protraction with forward flexion. Sports mostly associated with this injury are judo, karate, kickboxing, football, lacrosse and hockey. Symptoms generally have an insidious onset and are poorly localised.5–10 Subjects often present a vague posterior shoulder pain that may radiate down the radial axis of the arm, weakness of abduction and external rotation, and scapular winging. Most authors,11 considering that the SAN is only a motor nerve, attribute this pain to the placement of tension on the shoulder joint or elements of the brachial plexus secondary to chronic depression. However, other authors12 suggest the possible presence of nociceptive fibres, potentially responsible for the pain reported by some patient. In our case, the winging of the scapula was accentuated by arm abduction and external shoulder rotation against resistance and disappeared during forward flexion of the arm. Differently, in case of lesion of the long thoracic nerve, the lateral winging is worsened with forward flexion.13

Some authors suggested that strenuous exercise with the scapular girdle muscles might be the reason of spontaneous onset. They hypothesised that SAN palsy is the consequence of repetitive movements or muscular hypertrophy with strenuous work or sport training.4 Coulter and Warme published a case report where they describe a complete SAN palsy as a result of sustained compression from carrying climbing gear.14

As we know, the superficial location of SAN makes it vulnerable to direct blows to the neck or traction injuries. In our athlete, the history of a high-intensity weight training, during the period preciding the onset, with severe mechanical solicitations support our final hypothesis of a mechanical compression injury. In particular, that athlete performed a heavy power resistance training on a squat machine, where the weight lay on the trapezius muscle.

Another hypothesis could be the Parsonage Turner syndrome, an uncommon idiopathic neurological disorder characterised by rapid onset of severe pain followed by amyotrophy. However, in this syndrome, the pain has been described as sharp, aching, burning or stabbing, often worse during the evening or at night, with a recovery that can take months to years and sometimes is incomplete.15–17

Therefore, we suggest that the mechanical compression, due to shoulder braces of the weight machine, could have induced a transient palsy of the SAN, perhaps facilitated by a more superficial path of the nerve in this subject.

Patient’s perspective.

Given the difficulty of receiving a clear diagnosis, I was worried about the time of recovery from this injury and mostly about the chance of an incomplete recovery that could affect my sport career.

Learning points.

  • Spinal accessory nerve, due to its superficial course, can be injured during sports by traction or cross-body abduction or protraction with forward flexion, as well as by mechanical compression.

  • Team physicians and athletic trainers should be aware of the potential problems that can arise from incorrect or improper strength training (in this case involving upper body muscles).

  • The preseasonal period is often the most critical for injuries and all symptoms after training should never be undervalued, particularly in professional athletes exposed to very high-training loads.

  • The timing of instrumental evaluations (radiological or others) is critical to avoid potential mistakes and/or to improve the sensitivity of the exams.

Footnotes

Contributors: AE has been involved in the clinic management of this patient. AE, MB, SR and VB reviewed the details of the case, drafted the case report and contributed to the editing of the final product.

Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests: None declared.

Provenance and peer review: Not commissioned; externally peer reviewed.

Patient consent for publication: Obtained.

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